摘要
目的：探讨脑局部缺血后神经元损伤的分子机制。方法：经颞骨开窗结扎大鼠大脑中动脉，制成脑局部缺血模型，采用地高辛标记Ｃ－ｆｏｓ探针原位杂交法，观察脑缺血后大脑皮层及海马等区域Ｃ－ｆｏｓ基因的表达状况，用Ｃ－ｆｏｓ阳性细胞密度作定量研究指标。结果：脑缺血组、氯胺酮组和对照组，在大脑皮层及海马区域Ｃ－ｆｏｓ阳性细胞分别呈高密度、低密度和散在分布，三组间相差显著（Ｐ＜０．０１）。在脑的其余部位，包括丘脑、脑干、小脑等区域，三组Ｃ－ｆｏｓ阳性细胞均呈散在分布，无组间差异。结论：脑局部缺血可诱发大脑皮层及海马Ｃ－ｆｏｓ基因表达，Ｃ－ｆｏｓ基因表达可能是缺血致神经元损伤的分子机制之一；氯胺酮对脑缺血后Ｃ－ｆｏｓ基因表达有部分抑制作用；
Objective:To explore the moleculor mechanism of neuron damage after local cerebral ischemia. Method:Using the local cerebral ischemia model of rats made with thread embolism of middle cerebral artery, Cfos mRNA expression in rat brain was investigated by DIG labeled Cfos probe with in sites hybridization. Result:Cfos gene expression in cerebral cortex and hippocampus of ischemic group was significantly increased as compared with nonischemic group. Athough Cfos gene expression in ketamine treatedrat was also inreased ,yet it was significantly lower than that of ischemic group. Conclusion:Cfos expression in cerebral cortex and hippocampus can be induced by local cerebral ischemia and Cfos gene expression may be one of the pathological mechanism of cerebral ischemia on molecular level. Ketamine may partly a role in inhibition of Cfos gene expression following local cerebral ischemia.
出处
《卒中与神经疾病》
1998年第1期1-3,共3页
Stroke and Nervous Diseases
